Expression and function of CCL2/CCR2 in rat micturition reflexes and somatic sensitivity with urinary bladder inflammation

Arms, Lauren; Girard, Beatrice M.; Malley, Susan E.; Vizzard, Margaret A.

doi:10.1152/ajprenal.00139.2013

Cited by 48 publications

(71 citation statements)

References 83 publications

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“…Previous studies reported that inflammatory cytokines can cause sensitization of polymodal C-fibers and facilitate Aβ input to the spinal cord leading to overactivity of the bladder [20, 21]. Arms reported that CCL2 expression was elevated in CYP-induced cystitis in rat and blockage of its high-affinity receptor was associated with increased bladder capacity and decreased void frequency [22]. In our study, antimuscarinics attenuated the CCL2, CCL5, and IL-6 expressions and the BOO with antimuscarinics groups had significantly longer micturition interval.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Antimuscarinics on the Bladder Remodeling After Bladder Outlet Obstruction

Liu

Luo

Yang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Overactive bladder associated with bladder outlet obstruction (BOO) is a highly prevalent condition, which is usually treated with antimuscarinics. However, the potential effects of antimuscarinics on the structure and function of bladder have not been investigated thus far. Methods: Sprague-Dawley(R) rats accepted bladder neck obstruction surgery or sham surgery, and then received treatment of three different antimuscarinics (Solifenacin, Darifenacin, and Tolterodine) or vehicle. After 3, 6 and 12 weeks, the bladder function and structure were measured. The effect of antimuscarinics on cellular alteration in vitro was observed under mechanical stimulation. Bladder morphology were examined by immunohistochemistry, and the bladder function were investigated by cystometry and strip contractility test. The expression of muscarinic receptors and inflammatory cytokines were measured by PCR and Western blotting. Results: Here we demonstrate, both in vitro and in vivo, that antimuscarinics are protective regulators for the bladder structure and function. Antimuscarinics decrease the weight of bladders with BOO. Antimuscarinics improve the voiding parameter and enhance the contraction of bladder smooth muscle. The results also show that antimuscarinics inhibit the proliferation of bladder smooth muscle cells both in vivo and in vitro, it can reduce the collagen deposition and inflammatory cytokines in bladders with BOO. During this process, the expression of M2 and M3 receptors was altered by antimuscarinics. Conclusion: Antimuscarinics could reverse the structural and functional changes of BOO bladder wall at cellular and tissue level, and the alteration of M2 and M3 receptors may be involved in this biological process.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Antimuscarinics on the Bladder Remodeling After Bladder Outlet Obstruction

Liu

Luo

Yang

et al. 2017

Cell Physiol Biochem

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“…Bladder catheter implantation was performed in normal rats as previously described [7,9,13] . Briefly, rats were anesthetized by intraperitoneal injection of pentobarbital sodium (50 mg/kg).…”

Section: Intravesical Catheter Implantationmentioning

confidence: 99%

Urodynamic characteristics of awake rats under retrained versus freely moving condition: Using a novel model

Chen

Zhang

Tian

et al. 2016

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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Urodynamic investigation in conscious rats is widely employed to explore functional bladder disorders of various etiologies and pathogeneses. Rats can be placed in restraining cages or wide cabinets where they are allowed to move freely during cystometry. However, the requirements of special devices hampered the application of urodynamic test in freely moving rats, and whether the restraint has any effects on urodynamic parameters in conscious rats remains obscure. In the present study, we described a novel approach for urodynamic investigation in both restrained and freely moving conscious rats. In addition, we for the first time systematically compared the urodynamic parameters of rats in the two conditions. With the current method, we successfully recorded stable and repeatable intravesical pressure traces and collected expected reliable data, which supported the idea that the restraint does not affect the activity of the micturition reflex in rats, provided sufficient and appropriate measures could be applied during cystometry. Fewer technique problems were encountered during urodynamic examination in restrained rats than in freely moving ones. Taken together, conscious cystometry in rats placed in restraining cages with proper managements is a reliable and practical approach for evaluating the detrusor activity and bladder function.

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“…Intravesical instillation of 1 ml 0.01% DMSO in 0.9% NaCl under 2% isoflurane was used for the vehicle control conditions. Rats remained anesthetized during instillation to suppress the micturition reflex and prevent expulsion of SB505124 (5 M) or 0.01% DMSO (2,3,5). At the conclusion of drug instillation, urinary bladder function tests were repeated and run for at least six reproducible micturition cycles (postdrug).…”

Section: Cystometrymentioning

confidence: 99%

Expression and function of transforming growth factor-β isoforms and cognate receptors in the rat urinary bladder following cyclophosphamide-induced cystitis

Gonzalez

Girard

Vizzard

2013

American Journal of Physiology-Renal Physiology

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102

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Numerous proinflammatory cytokines have been implicated in the reorganization of lower urinary tract function following cyclophosphamide (CYP)-induced cystitis. The present study investigated the functional profile of three pleiotropic transforming growth factor-β (TGF-β) isoforms and receptor (TβR) variants in the normal and inflamed (CYP-induced cystitis) rat urinary bladder. Our findings indicate that TGF-β (1, 2, and 3) and TβR (1, 2, and 3) transcript and protein expression were regulated to varying degrees in the urothelium or detrusor smooth muscle following intermediate (48 h; 150 mg/kg ip) or chronic (75 mg/kg ip; once every 3 days for 10 days), but not acute (4 h; 150 mg/kg ip), CYP-induced cystitis. Conscious, open-outlet cystometry was performed to determine whether aberrant TGF-β signaling contributes to urinary bladder dysfunction following intermediate (48 h) CYP-induced cystitis. TβR-1 inhibition with SB505124 (5 μM) significantly (p ≤ 0.001) decreased voiding frequency and increased bladder capacity (2.5-fold), void volume (2.6-fold), and intercontraction intervals (2.5-fold) in CYP-treated (48 h) rats. Taken together, these results provide evidence for 1) the involvement of TGF-β in lower urinary tract neuroplasticity following urinary bladder inflammation, 2) a functional role of TGF-β signaling in the afferent limb of the micturition reflex, and 3) urinary bladder TβR-1 as a viable target to reduce voiding frequency with cystitis.

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Expression and function of CCL2/CCR2 in rat micturition reflexes and somatic sensitivity with urinary bladder inflammation

Cited by 48 publications

References 83 publications

Protective Effects of Antimuscarinics on the Bladder Remodeling After Bladder Outlet Obstruction

Protective Effects of Antimuscarinics on the Bladder Remodeling After Bladder Outlet Obstruction

Urodynamic characteristics of awake rats under retrained versus freely moving condition: Using a novel model

Expression and function of transforming growth factor-β isoforms and cognate receptors in the rat urinary bladder following cyclophosphamide-induced cystitis

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